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One major limitation in epilepsy research is that we have little understanding of the mechanism whereby seizures begin, known as ictogenesis. We have developed a novel model of ictogenesis, whereby we can modulate the endogenous seizure threshold by altering the afferent synaptic activity to an epileptic focus in rats with temporal lobe seizures. The method relies upon increasing the random activity of the nucleus reuniens, which sends a large number of afferent connections to the hippocampi. This increased synaptic noise pushes the hippocampus closer to seizure threshold.
We used a battery of qualitative and quantitative measurements to evaluate the induced seizures. Different animals had different seizures, but our injections produced seizures that were indistinguishable from the spontaneous ones.
The experimental protocol increased the risk of seizures nearly three-fold. We are using this model to identify biomarkers of ictogenesis, and to test the efficacy of antiseizure therapies.
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